Although it might be argued that the ability of metformin to interfere with the anaplerotic entry of glutamine into the TCA cycle can explain the increased sensitivity of BRCA1 one-hit cells to its anti-tumor initiating capacity, it should be also acknowledged that metformin reduced glucose-derived acetyl-CoA entry into mitochondrial metabolism in BRCA1 one-hit cells more dramatically than in BRCA1 wild-type cells. Here, BRCA1 is linked to neoplasm.